Hypoxia And Respiratory Failure

Question 1

What is the difference between hypoxaemia and hypoxia? When would you get hypoxia without hypoxaemia?

Answer 1

Hypoxaemia - low pO2 in blood

Hypoxia - O2 deficiency at tissue level

Hypoxia at tissues without hypoxaemia occurs in anaemia or in poor circulation

Question 2

What the normal O2 saturation and PaO2?

Answer 2

O2 saturation 94-98%

PaO2 9.3-13.3 KPa

When these levels are below LLN (lower limit of normal) defined as hypoxaemia

Question 3

When is tissue damage most likely? What is this used to diagnose?

Answer 3

O2 saturation <90%
PO2 <8KPA

This is used to diagnose respiratory failure - the clinical presentation will vary depending if it’s acute or chronic and an arterial blood gas may not always help to distinguish

Question 4

Causes of hypoxaemia

Answer 4

Low inspired O2 (drowning, high altitudes, hypoventilation (resp pump failure), ventilation/ perfusion mismatch, diffusion defect (problems alveolar capillary membrane), intra-lung shunt (acute respiratory distress syndrome) which is extreme V/Q mismatch, right to left shunt (cyanotic heart disease)

Question 5

Effects of hypoxaemia

Answer 5

Especially acute:

Impaired CNS function, confusion, irritability, agitation

Cardiac arrhythmias and cardiac ischaemia

Hypoxic vasoconstriction of pulmonary vessels -> pulmonary hypertension -> R heart failure + cor pulmonale (abnormal hypertrophy right heart)

Cyanosis (bluish discolouration of skin and mucous membranes due to presence of 4-6gm/dl of deoxyhaemoglobin)

Question 6

What are the two types of cyanosis?

Answer 6

Central cyanosis: seen in oral mucosa, tongue, lips indicates hypoxaemia - deoxygenated Hb in arteries <5 g/dl with O2 sats <85%

If ^^ present peripheral cyanosis will also be present

Peripheral cyanosis - fingers, toes, poor local circulation (more O2 extracted by the peripheral tissues)

Question 7

What occurs in chronic hypoxaemia as mechanisms to increase O2 delivery?

Answer 7

• increased EPOsecreted by kidneys -> raised Hb (polycythemia)
• increased 2,3 DPG shifts Hb saturation curve so O2 released more freely

Question 8

What’s the definition of type one and two respiratory failures?

Answer 8

Type 1 -Just low O2
low pO2 < 8kpa or O2 saturation <90% room air, PCO2 normal or low, gas exchange impaired at level of alveo-capillary membrane

Can progress to (disease progress and more of lung involved) …

Type 2 - low O2 & high CO2
Low PO2 & high PcO2 >6.5 KPa,
Respiratory pump failure e.g. hypoventilation

Difference: CO2 levels, cause

Question 9

What determines alveolar ventilation?

Answer 9

(Tidal volume - dead space) X respiratory rate

Question 10

Which type of respiratory failure would hypoventilation cause and why?

Answer 10

Type 2 as it always causes hypercapnia and hypoxaemia

Question 11

Causes of hypoventilation

Answer 11

End stage COPD (flattened diaphragm)

Asthma

Stabbing

Drug overdose (suppresses respiratory centre)

Head injury

Neuromuscular disease e.g. muscular dystrophy

End stage pulmonary fibrosis

Obesity (central in Brain or obstructive sleep apnoea and decreased lung space)

Question 12

Compare acute and chronic hypoventilation

Answer 12

Acute - urgent treatment, may need artificial ventilation, commonest causes: opiate overdose, head injury very severe acute asthma

Chronic - chronic hypoxaemia and hypercapnia, slow progression, time for compensation so better tolerated. Commonest causes: severe COPD, acute exacerbations may occur due to LRT infection

Question 13

What is scoliosis, kyphosis and kyphoscoliosis? Why can they all cause lung problems?

Answer 13

Scoliosis - sideways curvature of the spine

Kyphosis - XS outward curve results in abnormal rounding of the back ‘hunchback’

Kyphoscoliosis - both

Limit chest space so impaired ability for chest to expand

Question 14

Causes of respiratory failure

Answer 14

Opiates, head injury, trauma cervical spinal cord, Guillain-Barre syndrome, myasthenia gravis, pneumothorax, v severe acute asthma, foreign body

Causes of chronic type 2 only: myopathy, MD, end stage lung fibrosis, late stages of COPD, kyphoscoliosis

Could be more than one mechanism e..g lung fibrosis -> diffusion defect but if severe hypoventilation also OR pulmonary oedema -> diffusion defect and V/Q mismatch .

Question 15

Effects of hypercapnia

Answer 15

Respiratory acidosis

Impaired CNS function (drowsiness CO2 narcosis, confusion, coma, flapping tremors arms straight, wrist extended hands flap)

Warm hands, bounding pulse (peripheral vasodilation)

Cerebral vasodilation - headache

Chronic: respiratory acidosis compensates HCO3- kidney, acclimation to CNS effects, vasodilation mild pink puffers

Question 16

What occurs in central chemoreceptors with chronic CO2 retention?

Answer 16

CO2 diffuses CSF -> PH drops -> stimulates central chemoreceptors -> choroid plexus cells secrete HCO3- in CsF -> CSF PH normal

PCo2 I’m blood still high but central chemoreceptors unresponsive to this ‘reset to a new higher CO2 level’

Now main control is by peripheral chemoreceptors which detect PO2, respiratory drive now driven by hypoxia

Question 17

How could treatment of hypoxia worsen hypercapnia?

Answer 17

✅ give O2 improves PO2 so peripheral chemoreceptors stop hypoxic respiratory drive (resp rate and depth reduce) -> worsening hypercapnia

And

Correction of hypoxia removes hypoxic vasoconstriction leads increased perfusion of poorly ventilated alveoli and diverts blood away form better ventilated alveoli (V/Q mismatch)

Increasing CO2 May gradual, tel, by increasing blood HCO3-

So need to give controlled O2 therapy target 88-92% and can give ventilatory support

Question 18

What conditions could cause a V/Q mismatch?

Answer 18

conditions where SoME alveoli are poorly ventilated

O2 therapy

Asthma (variable airway narrowing)

RDS

Pulmonary oedema

Pulmonary embolism

Pneumonia (exudate in affected alveoli)

V/Q = <1 in these alveoli

-> hypoxic vasoconstriction occurs to try to divert some blood to better ventilated alveoli

If this fails..
-> hyperventilation

Question 19

What’s the final result of hyperventilation caused by a V/Q mismatch on PO2 and PcO2 and why?

Answer 19

Hyperventilation -> affected alveoli still poorly ventilated but unaffected segments increased ventilation:

PO2 rise and pCo2 falls
Increase O2 increased dissolved a little and once HB fully saturated (PO2 >10kPa) has no effect so overall doesn’t compensate for pathological segments

More CO2 dissolves or is transported as HCO3- so doesn’t rely as much on Hb saturation (only 30%)

So final result: low PO2 with normal/ low PCO2 = type one resp failure

Question 20

Which conditions will lead to a diffusion impairment at alveolar capillary membrane? What does this cause?

Answer 20

Fibrotic lung disease (thickened membrane and interstitium)

Pulmonary oedema (fluid increases diffusion distance)

CO2 less affected as more soluble so: Po2 low and PCO2 normal/ low until end stage = type one respiratory failure

Question 21

Causes of diffuse lung fibrosis and appearance on spirometry

Answer 21

Causes: idiopathic fibrosing alveolitis, asbestosis, extrinsic allergic alveolitis, pneumoconiosis

Reduced compliance, restrictive lung disease so restrictive pattern on spirometry (reduced FEV1 and FVC reduced on volume, time but no scalloping on expiratory flow rate, volume)

Partially correct hypoxaemia with O2 administration

Question 22

What is a shunt of the respiratory system? What’s a cause?

Answer 22

Some alveolar are perfused but not ventilated at all e.g. V/Q = 0

Acute respiratory distress syndrome

Question 23

What is acute respiratory distress syndrome? What does it cause? How can you manage it?

Answer 23

End result of acute alveolar injury caused by different insults e.g. damage to alveolar capillary unit -> increased vascular permeability, oedema, fibrin- exudation, heavy red lungs showing congestion and oedema (alveolar contain fluid and lined by hyaline membrane)

There is diffuse loss of surfactant -> alveolar atelectasis (collapse) -> lungs stiff and less compliant -> intrapulmonary shunt

Hard to manage on ventilator, always need to add positive pressure ventilation (PEEP)